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PubMed2004

Hypertensive Encephalopathy.

The term hypertensive encephalopathy should be reserved for patients with diffuse cerebral effects of precipitous and sustained rises in blood pressure that reverse when blood pressure is lowered and are not due to infarction or hemorrhage. The definitive diagnosis of this syndrome depends on accurate exclusion of other causes that may be associated with elevated blood pressure and neurologic deficits. Treatment is aimed at preventing or limiting target organ (brain) damage. Therapy should be individualized but centered on reducing the mean arterial blood pressure within a period of minutes to 2 hours, by no more than 20% to 25% or to a diastolic blood pressure of 100 to 110 mm Hg (whichever is higher), using short-acting intravenous agents. Oral or sublingual agents should generally be avoided in hypertensive encephalopathy because they are more likely to cause precipitous falls in blood pressure.

Journal Article↗
PubMed1981

Intracranial pressure monitoring in severe hypertensive encephalopathy.

Treatment of arterial hypertension in severe hypertensive encephalopathy does not always result in clinical improvement in the patient's central nervous system. In order to elucidate further the status of the brain, the authors have measured intracranial pressure (ICP) and arterial pressure in three cases of severe hypertensive encephalopathy. ICP was elevated in two of the three cases with peak values ranging from 32-70 mm Hg. In these 2 patients, therapy to lower ICP, including hyperventilation, steroids, barbiturates, and furosemide was begun early in the course. Cerebral perfusion pressure (CPP), defined as the difference between mean arterial pressure and ICP, was kept over 50 mm Hg to maintain adequate cerebral blood flow (CBF). These 2 patients survived. In the third case, measures to control ICP were instituted late in the course and the patient died of brain herniation. Intracranial hypertension is a complication of hypertensive encephalopathy and may contribute to cerebral injury. In cases of severe hypertensive encephalopathy, both ICP and arterial pressure should be monitored continuously. Judicious therapy aimed at lowering both ICP and arterial pressure, while maintaining an adequate CPP, should be employed.

Adolescent↗
PubMed1978

Hypertensive encephalopathy: recognition and management.

Hypertensive encephalopathy is a dramatic syndrome characterized by severe elevation of blood pressure, headache, visual disturbances, altered mental status, and convulsions. Although the syndrome is uncommon, to recognize and treat it promptly is important or the condition may prove to be fatal. Hypertensive encephalopathy should be distinguished from other cerebral complications of severe hypertension by obtaining careful history and performing thorough physical examination. The only definitive criterion for the diagnosis of this syndrome is its prompt response to therapy. If the patient's condition does not improve with hypotensive therapy, the physician should immediately search for alternate diagnoses. Potent drugs are available for prompt reduction of blood pressure. There are few medical emergencies in which the objective response to therapy is so strikingly apparent as in hypertensive encephalopathy.

Brain Diseases↗
PubMedDate not supplied

Computed tomographic changes of hypertensive encephalopathy.

Computed tomographic (CT) scans were evaluated in 11 patients with acute hypertensive encephalopathy. Hypertensive encephalopathy is characterized by an acute, severe rise in blood pressure associated with headache, nausea, vomiting, altered mental status, and focal neurologic deficits, and rapid improvement after control of blood pressure. The systolic blood pressure range is 200-280 mm Hg; diastolic is 130-170 mm Hg. The most common CT finding was white-matter edema, diffuse or focal, affecting the supratentorial compartment in all cases and the infratentorial compartment in eight. These changes resolved after the blood pressure was lowered in all six patients studied by follow-up CT. Permanent areas of infarction were demonstrated in three patients. These abnormalities are correlated with the neuropathologic findings in hypertensive encephalopathy.

Adolescent↗
PubMed1998

Diffusion-weighted MR imaging in hypertensive encephalopathy: clues to pathogenesis.

PURPOSE: Hypertensive encephalopathy, a complex of cerebral disorders, including headache, seizures, visual disturbances, and other neurologic manifestations, is associated with a variety of conditions in which blood pressure rises acutely. It has been ascribed to either exuberant vasospasm with ischemia/infarction or breakthrough of autoregulation with interstitial edema. Diffusion-weighted MR imaging may be used to determine whether the edema in hypertensive encephalopathy is cytotoxic or vasogenic in origin. METHODS: Diffusion-weighted imaging was performed using the double line scan diffusion imaging technique on a 1.5-T MR system. Seven patients with hypertensive encephalopathy were imaged within 1 day of the onset of their symptoms. Apparent diffusion coefficient maps as well as low and high b-factor images were acquired. The two-tailed paired Student's t-test was used to compare the apparent diffusion coefficients in edematous brain regions with those of normal white matter. RESULTS: In all cases the apparent diffusion coefficient maps of the patients with hypertensive encephalopathy showed increased signal in regions corresponding to increased T2 signal on standard T2-weighted (low b-factor) images. Quantitative apparent diffusion coefficients in regions of abnormal T2 signal were 1.36 +/- 0.14 microm2/ms, compared with 0.80 +/- 0.05 microm2/ms in normal white matter. Diffusion-weighted (high b-factor) T2-weighted images did not show abnormal signal. CONCLUSION: Diffusion-weighted MR imaging shows that the edema in hypertensive encephalopathy is of vasogenic origin and does not represent ischemia or infarction. This finding may have therapeutic implications.

Adult↗
PubMed1996

Parietal occipital edema in hypertensive encephalopathy: a pathogenic mechanism.

Eight patients with hypertensive encephalopathy from diverse etiologies developed cerebral edema in the vertebrobasilar distribution which resolved after blood pressure was lowered. Parietal occipital edema is a recognized feature of hypertensive encephalopathy. The explanation for this regional pathological variation in hypertensive encephalopathy remains undefined. Some evidence suggests that sympathetic innervation of the anterior cerebral vasculature may be protective, and conversely, the relative lack of sympathetic innervation in the vertebrobasilar vasculature may predispose the parietal occipital region to the development of cerebral edema in hypertensive encephalopathy.

Adolescent↗
PubMed2004

Hypertensive encephalopathy mimicking brainstem tumour in psychiatric patient.

Hypertensive encephalopathy is a syndrome consisting of headache, seizures, visual changes, and other neurologic disturbances in patients with elevated systemic blood pressure. Diagnosis based on clinical and radiological findings, which are not specific, may be difficult to establish. Furthermore, hypertensive encephalopathy may develop gradually even when blood pressure is lower than that of malignant hypertension. We present clinical, magnetic resonance imaging (MRI) and autopsy findings in a 43-year-old schizophrenic patient with unrecognised hypertensive encephalopathy, which was misinterpreted by MRI as a diffusely growing brain stem tumour. Increased blood pressure was recorded several times, but it was not properly controlled and treated either during his out-door psychiatric examinations or hospitalisation. At autopsy, generalised atherosclerosis, concentric hypertrophy of the left ventricle and arteriolonephrosclerosis were found in addition to microvascular fibrinoid necroses and thromboses in the brain and kidneys, which were almost certainly caused by arterial hypertension evolving from benign into malignant stage. We discuss the differential diagnosis and give a review of the literature.

Adult↗
PubMed1980

Hypertensive encephalopathy: a diagnosis of exclusion.

Patients with hypertension and altered neurologic status represent difficult diagnostic problems. If these patients are presumed to have hypertensive encephalopathy, specific diagnostic procedures and therapy may be delayed. Our case report and discussion emphasize the difficulty of differentiating hypertensive encephalopathy from other conditions and illustrate hypertensive encephalopathy should not be a primary diagnosis, but only a diagnosis of exclusion.

Aged↗
PubMed2006

Zonisamide eradicated paroxysmal headache with EEG abnormalities triggered by hypertensive encephalopathy due to purpura nephritic syndrome.

Generally, prognosis of hypertensive encephalopathy in childhood is favorable. We reported a 5-year-old girl who presented with a headache attack and EEG abnormalities after hypertensive encephalopathy due to purpura nephritis. The patient had suffered from hypertensive encephalopathy due to purpura nephritis, which soon ameliorated. Five months later, she developed attacks of headache, vomiting and disturbed consciousness with left side-predominant EEG abnormalities. Although carbamazepine and sodium valproate failed to improve her condition, zonisamide eradicated both the symptoms and EEG abnormalities, and an attack has not reoccurred for 5 years since completion of her treatment. It is noteworthy that delayed-onset complications can occur in child hypertensive encephalopathy, cases of which should be followed up prudently. Zonisamide should be considered for treatment of attacks of headaches with an epileptic character.

Anticonvulsants↗
PubMed2002

Hypertensive encephalopathy.

The case report of a patient with hypertensive encephalopathy is presented here. The findings of reversible bilateral thalamic changes on T2-weighted MR imaging is an atypical manifestation of the reversible posterior leucoencephalopathy syndrome (RPLS), which is the neuroradiological correlate of hypertensive encephalopathy. The importance of prompt and accurate diagnosis of hypertensive encephalopathy / RPLS is stressed.

Brain↗
PubMed1983

Hypertensive encephalopathy. A cause of neonatal seizures.

Hypertensive encephalopathy is rare in newborns. The few reported cases of malignant hypertension in newborns have been secondary to renovascular disease. We studied an infant with hypertensive encephalopathy secondary to isolated coarctation of the aorta. Infants with this condition are generally asymptomatic; to our knowledge, this is the youngest patient to have had neurologic complications secondary to isolated coarctation of the aorta.

Adult↗
PubMed1997

Hypertensive encephalopathy in children.

We present five cases of hypertensive encephalopathy in children, three with MR imaging findings and two with CT findings alone. One of the five patients had MR perfusion imaging, which showed perfusion abnormalities that support the concept of vasodilation as the major contributor to the syndrome. Hypertensive encephalopathy is rarely reported in children, and its true prevalence may be underestimated. Characteristic lesions in the severely hypertensive child should be recognized as manifestations of hypertensive encephalopathy, and subsequent clinical management should focus on treatment of the hypertension and/or its underlying causes.

Adolescent↗
PubMed2002

Plasma concentrations of atrial and brain natriuretic peptides in a case with hypertensive encephalopathy.

Hemodynamic mechanism for brain edema forrmation in patients with hypertensive encephalopathy is unclear. Potential roles of natriuretic peptides in the pathogenesis of hypertensive encephalopathy are discussed. A 32-year-old man presented with slight left hemiparesis. He was slightly confused, and his blood pressure was extremely high. Cranial plain computerized tomography scans revealed diffuse brain edema mainly in the supratentorial white matter region. Blood examination revealed that plasma concentrations of atrial and brain natriuretic peptides were significantly high. His left hemiparesis disappeared within a day, but he tended to be agitated. His altered mental status, however, resolved with control of blood pressure. Serial magnetic resonance imagings demonstrated that the magnitude of brain edema was attenuated in proportion to decline in plasma concentrations of natriuretic peptides. This case suggests that significant elevation of plasma concentrations of natriuretic peptides may contribute to an acute rise in blood pressure, and that these peptides potentially play an important role in development of brain edema in hypertensive encephalopathy.

Adult↗
PubMed1979

Atypical aspects of hypertensive encephalopathy in childhood.

Four patients with hypertensive encephalopathy and misleading focal symptomatology are reported in order to point out the problems of differential diagnosis. The first patient, together with a classical syndrome of hypertensive encephalopathy, had peculiar EEG features consistent with a possible diagnosis of herpes simplex encephalitis. Case 2 presented with a complex clinical syndrome associating bizarre spells suggestive of a psychiatric condition with ocular symptoms pointing to an upper brain stem involvement. The third child was remarkable because of the presence of neuroradiological signs compatible with a space-occupying lesion of the posterior fossa not eventually found after a surgical exploration performed as an emergency procedure. The last patient had central nervous system signs in the context of a Guillain-Barré syndrome: in this case the central symptomatology would not fit the already described pattern of encephalomyelo-radiculo-neuropathy but had to be entirely ascribed to the ill controlled arterial hypertension.

Adolescent↗
PubMed1988

[Neuropathology of hypertensive encephalopathy].

An account is given of hypertensive encephalopathy on the basis of neurohistological studies into 54 brains, with additional reference being made to autopsies. Vasculopathy of peripheral arteries and arterioles along with thickening of vascular walls, change of media, and lumen stenosis were primarily recorded by means of optical light and electron microscopy. A difference of more than seven per cent was found to exist between wall thicknesses of arterioles in hypertensive brains, on the one hand, and those in normotensive brains, on the other. Vessels with thickened walls were not rigid but were rather capable of dilation just as under normotensive conditions. Their inner diameters, however, were below normal. Vascular wall fibrosis, to which little attention had been given in the past, was repeatedly recordable from the venous and capillary systems. Impairment of the endothelial barrier function was quite often recorded, with lipid deposits being incorporated in peripheral arterioles and capillaries. No relevance to pathogenesis can be reliably attributed at present to detection of IgG in the arterial system. Microinfarction, micro-haemorrhage as well as disseminated damage to nerve cells are recordable from roughly one third of all hypertensive brains and are primarily located in brain stem ganglia. Demyelinisation and cerebral oedema are quite infrequent. High-protein cerebral oedema was found in some rare cases. Hypertensive encephalopathy should be considered as a nosological entity in which morphological and clinical phenomena are not always correlated to each other.

Arterioles↗
PubMed2006

[Hypertensive encephalopathy: differential diagnosis of brain edema with midline shift].

Hypertensive encephalopathy is a severe complication of hypertensive crisis or malignant hypertonia. We report a case with grave clinical and radiological features. The patient was comatose, with pupillary dysfunction, and initial CT suggested a local intracranial mass with edema. Cranial MRI showed almost completely hyperintensive supratentorial white matter, with edema and midline shift, and hypertensities in cerebellum and brainstem. The patient recovered, and the radiological findings improved after antihypertensive therapy. Hypertensive encephalopathy may be differentiated by MRI, manifests acutely, and is potentially reversible when adequate therapy is rapidly performed.

Anisocoria↗
PubMed1992

Hypertensive encephalopathy: findings on CT, MR imaging, and SPECT imaging in 14 cases.

Hypertensive encephalopathy is a syndrome consisting of headache, seizures, visual changes, and other neurologic disturbances in patients with elevated systemic blood pressure. The purpose of this study was to analyze the imaging findings in 14 patients with hypertensive encephalopathy. CT (n = 13), MR (n = 12), and single-photon emission computed tomography (n = 2) examinations performed in these patients before and after resolution of symptoms were reviewed. Eight had the preeclampsia-eclampsia syndrome, and six had hypertensive encephalopathy due to other causes. CT and MR findings in all patients having these examinations were indicative of edema in the cortex and subcortical white matter in the occipital lobes. Two of the 14 patients also had similar findings in the cerebellum and frontal lobes. Single-photon emission computed tomography showed increased vascular perfusion adjacent to areas that appeared abnormal on CT and MR. The findings on the imaging studies resolved on follow-up examinations performed after the hypertension was corrected. Our results suggest that the radiologic findings associated with hypertensive encephalopathy may be useful in establishing the diagnosis in the appropriate clinical setting.

Adolescent↗